Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway

Dong, Peixin; Xiong, Ying; Konno, Yosuke; Ihira, Kei; Kobayashi, Noriko; Yue, Junming; Watari, Hidemichi

Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway

Dong, Peixin; Xiong, Ying; Konno, Yosuke et al.

Journal of Experimental & Clinical Cancer Research, 2021, 40, 216

Permalink : https://hdl.handle.net/2115/82149

このアイテムのアクセス数:639件（2026-10-06 07:23 集計）

閲覧可能ファイル

ファイル	フォーマット	サイズ	閲覧回数	説明
Final published DLEU2 2021-6-28	pdf	5.94 MB	458

論文情報

ファイル出力 EndNote Basic出力 Mendeley出力

アクセス権	open access
URI	https://hdl.handle.net/2115/82149
タイトル	Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway
著者	Dong, Peixin ; Xiong, Ying ; Konno, Yosuke ; Ihira, Kei ; Kobayashi, Noriko ; Yue, Junming ; Watari, Hidemichi
e-Rad_Researcher 50602504 著者名 Dong, Peixin
著者名 Xiong, Ying
著者名 Konno, Yosuke
著者名 Ihira, Kei
著者名 Kobayashi, Noriko
著者名 Yue, Junming
著者名 Watari, Hidemichi
言語	英語
キーワード	HK2
	FAK
	ERK1/2 signaling
	DLEU2
	Long noncoding RNA
	LncRNA
	MicroRNA
	EMT
	Aerobic glycolysis
	Endometrial cancer
発行日	2021-06-26
収録物名	Journal of Experimental & Clinical Cancer Research
巻(号)	40
ページ	216
抄録	Background: Epithelial-to-mesenchymal transition (EMT) and aerobic glycolysis are fundamental processes implicated in cancer metastasis. Although increasing evidence demonstrates an association between EMT induction and enhanced aerobic glycolysis in human cancer, the mechanisms linking these two conditions in endometrial cancer (EC) cells remain poorly defined. Methods: We characterized the role and molecular mechanism of the glycolytic enzyme hexokinase 2 (HK2) in mediating EMT and glycolysis and investigated how long noncoding RNA DLEU2 contributes to the stimulation of EMT and glycolysis via upregulation of HK2 expression. Results: HK2 was highly expressed in EC tissues, and its expression was associated with poor overall survival. Overexpression of HK2 effectively promoted EMT phenotypes and enhanced aerobic glycolysis in EC cells via activating FAK and its downstream ERK1/2 signaling. Moreover, microRNA-455 (miR-455) served as a tumor suppressor by directly interacting with HK2 mRNA and inhibiting its expression. Furthermore, DLEU2 displayed a significantly higher expression in EC tissues, and increased DLEU2 expression was correlated with worse overall survival. DLEU2 acted as an upstream activator for HK2-induced EMT and glycolysis in EC cells through two distinct mechanisms: (i) DLEU2 induced HK2 expression by competitively binding with miR-455, and (ii) DLEU2 also interacted with EZH2 to silence a direct inhibitor of HK2, miR-181a. Conclusions: This study identified DLEU2 as an upstream activator of HK2-driven EMT and glycolysis in EC cells and provided significant mechanistic insights for the potential treatment of EC.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
権利情報	Creative Commons Attribution 4.0 International
PISSN	1756-9966
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.1186/s13046-021-02018-1